Premenstrual Syndrome (PMS) is characterized by the cyclic recurrence of a variety of emotional and physical symptoms that occur before menses and subside with the onset of menstruation. The temporal occurrence of these symptoms during the luteal phase, rather than their nature, seems to define this phenomenon. The precise pathophysiology remains conjectural and obscure, although much has been written. Symptoms can range from mild to incapacitating. It has been estimated that as much as 90% of all premenopausal women have some degree of premenstrual symptoms and approximately 10 to 20% have severe and incapacitating symptoms. This latter population has been estimated to be about 7 million women.
Numerous hypotheses have been proposed to explain the underlying pathophysiology in PMS. These have included hormonal imbalances such as estrogen excess, progesterone deficiency, fluid retention, allergies, and alteration of endogenous opiates. Multiple therapeutic modalities have been prescribed without scientific foundation and without any significant clinical success.
Recently however, substantial success in this area has been achieved. For example, U.S. Pat. No. 4,946,679 to Thys-Jacobs teaches a method for the treatment of PMS by administering a therapeutically effective dose of calcium to an individual manifesting symptoms of PMS. Calcium plays a role in the release of neurotransmitters, endocrine and exocrine products, in the contraction of skeletal and smooth muscle, and metabolism. Menstruation is related to ovarian and pituitary secretory function. The '679 patent discloses that calcium, coupled with ovarian linked hormones, may modulate the intrinsic feedback mechanisms that translate physiologic neuroendocrine and hormonal messages into behavioral and somatic changes.
While calcium is very important in reducing the symptomalogy of PMS of most PMS sufferers, the clinical trial discussed herein reveals that vitamin D also has a role in the pathophysiology of PMS for those women who demonstrate low vitamin D levels.